FISCHER, MB., HM. WOLF, I. HAUBER, H. EGGENBAUER, Vojtěch THON, M. SASGARY and MM. EIBL. Activation via the antigen receptor is impaired in T cells, but not in B cells from patients with common variable immunodeficiency. EUROPEAN JOURNAL OF IMMUNOLOGY. 1996, vol. 26, No 1, p. 231-237. ISSN 0014-2980.
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Basic information
Original name Activation via the antigen receptor is impaired in T cells, but not in B cells from patients with common variable immunodeficiency
Name in Czech Aktivace cestou antigenního receptoru je porušena u T buněk, avšak ne u B buněk pacientů s běžnou variabilní imunodeficiencí
Authors FISCHER, MB. (40 Austria), HM. WOLF (40 Austria), I. HAUBER (276 Germany), H. EGGENBAUER (40 Austria), Vojtěch THON (203 Czech Republic, guarantor), M. SASGARY (40 Austria) and MM. EIBL (40 Austria).
Edition EUROPEAN JOURNAL OF IMMUNOLOGY, 1996, 0014-2980.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 30102 Immunology
Country of publisher United States of America
Confidentiality degree is not subject to a state or trade secret
RIV identification code RIV/00216224:14110/96:00035801
Organization unit Faculty of Medicine
UT WoS A1996UD13800035
Keywords (in Czech) TCR; CVID
Keywords in English T cell activation; common variable immunodeficiency; T cell receptor; inositol phosphates
Tags common variable immunodeficiency, inositol phosphates, T cell activation, T cell receptor
Tags International impact, Reviewed
Changed by Changed by: prof. MUDr. Vojtěch Thon, Ph.D., učo 2483. Changed: 26/6/2009 00:18.
Abstract
The patients included in this study belong to a subset of common variable immunodeficiency (CVID) patients whose peripheral blood T cells have a T cell receptor (TCR)-mediated activation defect leading to impaired expression of the interleukin (IL)-2 gene upon stimulation with recall antigens (tetanus toxoid, Escherichia coli) or superantigens (staphy lococcal enterotoxins). In the present report we demonstrate that the patients' peripheral blood T cells failed to generate the second messenger inositol 1,4,5-trisphosphate (Ins(1,4,5)P-3) following stimulation with superantigen or mAb specific for the monomorphic region of the TCR beta-chain. Patients' T cell lines were also impaired in generating Ins(1,4,5)P, when stimulated with tetanus toxoid-pulsed autologous monocytes. Addition of a second or third co-stimulatory signal provided by recombinant IL-2, CD28 or both had no effect on the Ins(1,4)P-3 formation of the patients' antigen-driven T cell lines. The T cell activation defect, however, was not absolute, as Ins(1,4,5)P-3 formation in the patients T cells after phytohemagglutinin or aluminium fluoride stimulation was normal. The impairment in signal transduction via the T cell antigen receptor was limited to the patients' T cells, as no activation defect after ligation of surface immunoglobulin. the antigen receptor on B cells, could be detected.
Abstract (in Czech)
Aktivace cestou antigenního receptoru je porušena u T buněk, avšak ne u B buněk pacientů s běžnou variabilní imunodeficiencí.
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